Hypocortisolism leads to an increase in adrenocorticotropic hormone (ACTH) with consequent bilateral adrenal hyperplasia, accumulation of cortisol precursors (progesterone and 17α-OHP) and a shift towards the androgen production pathway (DHEA, androstenedione and testosterone).(1,6,7). Here, POMC is linked to congenital adrenal hyperplasia.